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Related Experiment Videos

Quantitative decrease in synaptophysin message expression and increase in cathepsin D message expression in Alzheimer

L M Callahan1, W A Vaules, P D Coleman

  • 1Department of Neurobiology & Anatomy, University of Rochester, New York 14642, USA.

Journal of Neuropathology and Experimental Neurology
|April 10, 1999
PubMed
Summary
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Alzheimer disease (AD) causes reduced synaptic gene expression in neurons with neurofibrillary tangles (NFTs). This selective gene expression change, particularly for synaptophysin, indicates NFTs disrupt neuronal function.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Alzheimer disease (AD) is characterized by neurofibrillary tangles (NFTs) and neuronal dysfunction.
  • Altered gene expression within affected neurons is a proposed mechanism in AD pathogenesis.

Purpose of the Study:

  • To investigate changes in gene expression within individual neurons affected by NFTs in the Alzheimer disease hippocampus.
  • To determine if NFT formation selectively impacts the expression of synaptic and lysosomal proteins.

Main Methods:

  • Combined immunocytochemistry and in situ hybridization techniques.
  • Quantified messenger RNA (mRNA) grain density for synaptophysin and cathepsin D in hippocampal CA1 pyramidal neurons.
  • Compared NFT-containing neurons with adjacent NFT-free neurons.

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Main Results:

  • Synaptophysin mRNA density decreased by 50% in NFT-containing neurons compared to NFT-free neurons.
  • Cathepsin D mRNA density increased by 33% in NFT-containing neurons.
  • Polyadenylated mRNA density decreased by 25% in NFT-containing neurons.
  • A negative correlation was found between the percentage of cell body occupied by NFT and synaptophysin mRNA density (r = -0.35, p < 0.0001).

Conclusions:

  • NFT formation is associated with selective alterations in gene expression profiles within individual neurons.
  • These findings suggest that events related to NFT formation may lead to reduced expression of synaptic messages, contributing to neuronal dysfunction in Alzheimer disease.